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EV ACVD Study > Vasculitis, Ischemic Dermatopathy, Panniculitis > Flashcards

Vasculitis, Ischemic Dermatopathy, Panniculitis Flashcards

1
Q

Breeds with familial vasculitis (all in puppies)

A

1) Beagles (familial necrotizing arteritis). ANCA positive.

2) GSD Familial Cutaneous Vasculopathy. Autosomal recessive. 2’ vaccination? Foot pads, nasal bridge. Self recover, but relapse with future vax.

3) Jack Russel Terrier Familial Cutaneous Vasculopathy. Vaccination? Ulcers, alopecia on boney prominences, pinnae, footpads.

4) Scottish Terrier Hereditary Vasculitis (pyogranuloma and vasculitis of the nasal planum); Autosomal dominant. Ulcer of nasal planum.

5) Shar Pei Vasculitis (life threatening! Idiopathic. Fever, hemorrhagic papules, deep ulcers, epidermal detachment. Tx GC)

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2
Q

Cryoglobulinemia causes

A

*Lead poisoning
*Upper respiratory infections
*Neoplasia (Multiple Myeloma, Lymphoma)
*Idiopathic

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3
Q

Systemic signs of cryoglobulinemia

A

*IMHA (IgM triggers it)
*Glomerulonephritis
*Thrombosis

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4
Q

Diagnosing cryoglobulinemia

A

*Immune complexes will be more severe in cold blood (refrigerator) and dissolve in warm temperature

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5
Q

Urticarial vasculitis causes

A

*Drugs
*CAFR
*Insects
*Cold
*Idiopathic

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6
Q

How to discern regular urticaria vs urticarial vasculitis

A

Vasculitic form will NOT blanch on diascopy

Normal urticaria WILL blanch on diascopy

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7
Q

Neonatal vasculitis pathogenesis

A

Foal ingesting anti-neutrophil and anti-platelet antibodies via colostrum –> forms immune complexes in their body (<4 days old) –> start bleeding.

Tx with GCs for 2 weeks. Usually a good prognosis.

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8
Q

Solar vasculitis skin color

A

Unpigmented, lightly pigmented

Often coexists with fDLE, vitiligo

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9
Q

Traction alopecia causes

A

Owners putting on cosemetic to tie the hair back (Rubber bands, Barrettes)

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10
Q

Traction alopecia lesions

A

Alopecia, thinning, scar –> well demarcated

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11
Q

Traction alopecia histopath

A

Follicular atrophy Deep arteritis (hyalinization of vessel wall)

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12
Q

Traction alopecia treatment

A

No self cure. Neglect vs pentoxifylline vs surgery

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13
Q

Cutaneous and Renal Glomerular Vasculopathy (AKA “alabama rot”: Breed

A

Racing greyhounds in USA

Many breeds in UK

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14
Q

Cutaneous and Renal Glomerular Vasculopathy (AKA “alabama rot”: etiology

A

E coli Shiga toxin (verotoxin) in raw beef

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15
Q

Cutaneous and Renal Glomerular Vasculopathy (AKA “alabama rot”: seasonality

A

Winter and summer in USA
Nov-May in the UK

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16
Q

Cutaneous and Renal Glomerular Vasculopathy (AKA “alabama rot”: pathogenesis

A

Thrombotic microangiopathy –> ischemia

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17
Q

Cutaneous and Renal Glomerular Vasculopathy (AKA “alabama rot”: clinical signs

A

Acute, with rapid deterioration

Edema, erythema –> hemorrhage, ulcers

HINDlimbs, footpads, mucosae

25% get acute kidney injury AKI. Usually AKI happens AFTER skin lesions.

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18
Q

Cutaneous and Renal Glomerular Vasculopathy (AKA “alabama rot”: Labwork findings

A

THROMBOCYTOPENIA (d/t consumption of platelets due to massive thrombosis)

AKI signs

Proteinuria, casts

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19
Q

Cutaneous and Renal Glomerular Vasculopathy (AKA “alabama rot”: treatment

A

If only skin lesions– self cure slowly, goof prognosis

Severe AKI: usually poor prognosis –> euthanize

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20
Q

Non-immune mediated causes of vasculitis (8)

A

1) Direct invasion of vascular wall (microorganisms, neoplasia)
2) Embolism (septic embolism)
3) Irradiation (UV)
4) Heat (thermal burns)
5) Water (equine immersion foot syndrome)
6) Trauma, irradiation (IV catheter)
7) Toxins
8) Hemodynamic factors (turbulence)

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21
Q

Immune mediated causes of vasculitis (4)

A

1) Immune complexes
*Antigen-antibody complexes –> complement (C3a, C5a, MAC) –> neutrophils –> granule contents, ROS released –> vasculitis

2) Anti-neutrophil cytoplasmic antibodies (ANCA)
*Ab binds to neutrophil –> activation –> granule contents, ROS released –> vasculitis
*Usual ANCA targets = neutrophil proteinase 3 & Myeloperoxidase

3) Anti-endothelial cell antibodies

4) T cells (CD8 autoreactive cells, NK cells), macrophages (ie FIP, Leishmania)

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22
Q

Main causes of vasculitis, general

A

Infection**
**Drug
*Immune-mediated dz
*CAFR
*Neoplasia
*Environmental factors (contact, heat, cold)

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23
Q

Proliferative (dermal) arteritis of the nasal philtrum: Breed

A

Saint Bernard

*Basset hound
*Bloodhound
*Dobie
*GSD
*Other large/giant breeds

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24
Q

Proliferative (dermal) arteritis of the nasal philtrum: Age

A

Mean 5 yr

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25
Q

Proliferative (dermal) arteritis of the nasal philtrum: Cause

A

Idiopathil

Familial predisposition in Saint Bernard

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26
Q

Proliferative (dermal) arteritis of the nasal philtrum: Clinical signs

A

Circular ulcer on nasal philtrum

1/3 of dogs will have PERFUSE bleeding from the lesion

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27
Q

Proliferative (dermal) arteritis of the nasal philtrum: Histopathology

A

Proliferative arteritis (deep arteries, arterioles)– Thickening of tunica media/intima: myofibroblasts that produce collagen/mucin around the arteries

Tunica interna: elastic lamina failure

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28
Q

Proliferative (dermal) arteritis of the nasal philtrum: Treatment

A

Prednisone, tacrolimus

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29
Q

Proliferative thrombovascular necrosis of the pinna: treatment

A

Oclacitinib!

30
Q

Proliferative (dermal) arteritis of the nasal philtrum: etiology

A

Idiopathic!!

Potentially vaccination, fenbendazole

31
Q

Proliferative (dermal) arteritis of the nasal philtrum: Predisposed pinnae

A

Pendulous, folded ears&raquo_space; Erect ears

32
Q

Proliferative (dermal) arteritis of the nasal philtrum: differential diagnoses

A

*Leishmania
*Bartonella henselae
*Frostbite
*Cryoglobulinemia-Cryofibrinogenemia
*Familial vasculopathies (GSD, JRT)
*Ischemic dermatopathies

33
Q

Ischemic Teat Necrosis (cows): etiology

A

Unknown.

Usually during 1st lactation cycle of cow

LOSS OF TEATS- necrosis, self trauma

34
Q

Types of Ischemic Dermatopathy (5)

A

1) Familial dermatomyositis
2) Dermatopmyositis-like in atypical breeds, Juvenile-onset ischemic dermatopathy
3) Post-rabies vaccine vasculitis and panniculitis
4) Generalized vaccine-associated ischemic dermatopathy
5) Adult-onset generalized idiopathic ischemic dermatopathy

35
Q

Ischemic dermatopathy: histopath

A

Cell poor interface dermatitis

*Basal cell: Hydropic degeneration, basal cell apoptosis. Suprabasilar vesicles, ulcers
Pigmentary incontinence
*Hair follicles: Hydropic degeneration, apoptosis –> atrophy, fibrosis
*Dermis: Collagen pallor, mucinosis, edema, fibrosis
*Blood vessels: vasculitis (occasional), endothelial loss, mural hyaline changes

36
Q

Ischemic dermatopathy differential diagnosis on histopath

A

Lupus

37
Q

Familial dermatomyositis: breed

A

Collie (rough), Shetland sheepdog

38
Q

Familial dermatomyositis: age

A

<6 months old for skin
Older for myositis

39
Q

Familial dermatomyositis mode of inheritance

A

NOT mendelian inheritance (used to be thought autosomal dominance. But MANY genes!)

40
Q

Familial dermatomyositis: genes

A

Risk alleles:
*PAN2
*MAP3K7CL polymorphisms
*MHC cl II haplotypes

41
Q

Familial dermatomyositis: environmental factors

A

*Estrus
*Sun exposure
*Trauma

*?? virus, vaccine, drugs, toxins, stress

42
Q

Familial dermatomyositis: antibody quantity

A

*Increased total IgG
*Increased circulating immune complexes (w/ IgG)

43
Q

Familial dermatomyositis: complement related?

A

No difference in complement quantities in dogs

But in humans, complement deficiency is important for dermatomyositis

44
Q

Familial dermatomyositis: clinical lesions, distribution

A

Alopecia, erythema, dyspigmentation, ulcers, scars, scale

Skin, footpads, nails; oral mucosa

45
Q

Familial dermatomyositis: which muscles are involved

A

Masseter > skeletal

Atrophy
Dysphagia
Regurgitation
Stiff gait

46
Q

Familial dermatomyositis: nail lesions

A

*Onychorrhexis
*Onychoschizia
*Onychomadesis

47
Q

Which breed has more myositis? Collies or Shelties?

A

Shelties

48
Q

Familial dermatomyositis: progression of disease

A

*Skin lesions worst at 1 year old
*Wax/wane clinical signs (stressful periods)
*May spontaneously cure, or PR

49
Q

Familial dermatomyositis: how to assess muscle involvement

A

*CK levels (only elevated if acute flare of myositis)
*Electromyography
*Muscle biopsy (atrophy, necrosis, fibrosis, mixed inflammation)

50
Q

Familial dermatomyositis: treatment

A

*Avoid triggers (sun, trauma; spaying if estrus trigger)
*Topical GC, tacrolimus
*Systemic GC, cyclosporine, MMP, pentoxifylline, vit E, OFA, doxycycline/niacinamide *Apoquel (works for other ischemic dermatopathies!) –> inhibition of Type 1 IFNs (which are a major cytokine for dermatomyositis)

51
Q

Non-familial ischemic dermatopathies (Juvenile, adult onset, vaccine-associated [local, generalized]): signalment

A

*SMALL DOGS > MEDIUM DOGS
*64% of dogs are <10kg!!
*Age: all

*Chihuahua
*Toy/Mini poodle
*Maltese

*Chinese crested
*Fox terrier
*Jack russel terrier
*Yorkshire terrier
*Schipperke
*Rat terrier

52
Q

Non-familial ischemic dermatopathies (Juvenile, adult onset, vaccine-associated): vaccine-associated signalment

A

*Toy poodle
*Young dogs
*Larger size dogs

53
Q

Non-familial ischemic dermatopathies (Juvenile, adult onset, vaccine-associated): localized vaccine-associated timeline

A

2-3 months (up to 8 mo) after rabies vaccine
*IgG and Rabies Antigen can be found in vessels and hair follicles!!!

54
Q

Non-familial ischemic dermatopathies (Juvenile, adult onset, vaccine-associated): Generalized vaccine-associated timeline

A

*up to 5 months after localized lesion (but don’t NEED a localized lesion first)

*C5b-9 membrane attack complex in muscle vessels

55
Q

Sterile nodular panniculitis breeds

A

Dachshunds
Poodles

Australian shepherds
Bristtany spaniels
Chihuahuas
Dalmation
Pomeranians

56
Q

Body regions for sterile nodular panniculitis

A

Neck, trunk

57
Q

Other systemic signs that may be related to sterile nodular panniculitis

A

IMPA

58
Q

Histo patterns of panniculitis

A

*Nodular
»>
*Septal
*Diffuse
*Intralobar

59
Q

Treatment for sterile nodular panniculitis

A

*GC + 2’ immunosuppressive agent
*Needed lifelong

Only 15% achieve CR with GC monotherapy

60
Q

Most common disease associated with cutaneous vasculitis in horses

A

Photo-aggravated dermatitis

(non-pigmented skin, normal liver enzymes, no exposure to photosensitizing agents)

BUT previous studies indicate Purpura hemorrhagica (2’ Streptococcus equi or Corynebacterium pseudotuberculosis). SQ limb edema; MM hemorrhage.

61
Q

Breed with higher rate of cutaneous vasculitis in horses

A

Paints
Pintos

(more unpigmented skin)

62
Q

Signalment with LOWER rates of cutaneous vasculitis in horses

A

Thoroughbreds
Stallions

63
Q

Most commonly affected site for cutaneous vasculitis in horses

A

Legs (crust, scale, edema)

64
Q

What clinical sign is indicative of a poorer prognosis in horses with cutaneous vasculitis

A

Fever

65
Q

T or F: Vasculitis can occur 2’ PF and equine sarcoidosis

A

True.

Antigenic stimulation cause those 2 diseases. If antigen is similar to vascular endothelium– vasculitis will occur
OR
Antigenic stimulation causes antigen-antibody complex deposition

66
Q

What type of hypersensitivity reaction occurs to trigger purpura hemorrhagica in horses

A

Type 3. Antibody-antigen complexes that deposit in vessel walls

67
Q

Labwork findings in horses with cutaneous vasculitis

A

Anemia
Neutrophilia
Hyperglycemia
Hyperglobulinemia

(2’ inflammation, stress, GC administration)

68
Q

T or F: Cutaneous vasculitis is likely to recur in horses

A

True. 44% have recurrence

69
Q

Most common treatments for cutaneous vasculitis in horses

A

TMS
Corticosteroids
Pentoxifylline (antiinflammatory, rheological)

70
Q

Factors associated with worse prognosis for ischemic dermatopathy in dogs

A

*<10kg
*increased age
*More lesion sites
*Systemic signs
*Pinnae, paw pad lesions

70
Q

Dermatomyositis genes

A

MAP 3K7CL
PAN2

EV ACVD Study (52 decks)

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